Rubia cordifolia · PhytoNexus

01 Identity and provenance

Accepted binomial: Rubia cordifolia
Common names: Manjistha
Family (APG IV): Rubiaceae
Part used: Root
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Reference not supplied - claim unverified against primary literature.

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Anthraquinones, Naphthoquinones, Triterpenoids	Alizarin, Purpurin, Munjistin, Rubiadin, Mollugin, Lucidin, Damnacanthal, Ruberythric acid, Pseudopurpurin, Anthraquinone glycosides Root	Mitoxantrone, Pixantrone, Doxorubicin (anthracycline analogue), Anthraquinone derivatives; Piroxicam, Celecoxib (functional anti-inflammatory similarity)

The analogue column is what makes the interaction reasoning tractable: where a constituent has a marketed structural counterpart, the counterpart's interaction profile is the starting hypothesis for the plant.

Looking up structures and physicochemical properties from PubChem…

03 Stated application

Reported activity: Anti-inflammatory, wound healing, antioxidant, hepatoprotective, antimicrobial, anti-acne, anti-arthritic, blood purifier, anticancer (experimental)
Marketed in: Ayurvedic capsules, blood purifier syrups, skin creams, wound healing ointments, anti-acne gels, polyherbal tablets, herbal cosmetics
Reported adverse effects: Gastrointestinal upset, nausea, abdominal discomfort, allergic skin reactions, possible increased bleeding risk with anticoagulants (theoretical), limited pregnancy safety data

04 Interaction matrix

Source column, verbatim: Anticoagulants/antiplatelets, NSAIDs, antihypertensives, hypoglycemic drugs, immunosuppressants, chemotherapeutic agents
Normalised onto 7 canonical drug classes below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Cytotoxic and targeted anticancer drugs Oncology	4Contraindicated	PK-CYP3A4/UGT + PD-antagonistic	curated B	Neutropenic sepsis and severe diarrhoea from over-exposure, or reduced an…	why ▾
Class mechanism. Botanical CYP3A4 and UGT1A1 modulation alters exposure to irinotecan, taxanes, vinca alkaloids and kinase inhibitors. High-dose antioxidant botanicals may also oppose the oxidative mechanism of some cytotoxics and of proteasome inhibitors. Expected Neutropenic sepsis and severe diarrhoea from over-exposure, or reduced antitumour effect; boronic-acid proteasome inhibitors are directly antagonised by polyphenols. Management No botanical should be taken during active cytotoxic therapy without oncology sign-off. Record all supplements in the chemotherapy chart. Onset unspecified Evidence B - reviewed clinical column, source pending Matched on “chemotherapeutic agents” Find evidence for this pair Map this mechanism
Immunosuppressants (ciclosporin, tacrolimus, mycophenolate) Transplant	4Contraindicated	PK-CYP3A4/P-gp + PD-antagonistic	curated B	Acute graft rejection with inducers; nephrotoxicity, neurotoxicity and hy…	why ▾
Class mechanism. These are narrow-therapeutic-index CYP3A4 and P-glycoprotein substrates. Botanical induction collapses trough levels; inhibition causes toxic accumulation. Immunostimulant botanicals separately oppose the therapeutic goal. Expected Acute graft rejection with inducers; nephrotoxicity, neurotoxicity and hypertension with inhibitors; autoimmune flare with immunostimulants. Management Treat as contraindicated in transplant recipients. Any exposure requires immediate trough level measurement and transplant team notification. Onset unspecified Evidence B - reviewed clinical column, source pending Matched on “immunosuppressants” Find evidence for this pair Map this mechanism
Anticoagulants (vitamin-K antagonists, DOACs) Haemostasis	3Major	PD-additive + PK-CYP2C9	curated B	INR destabilisation in either direction; ecchymosis, epistaxis, gum bleed…	why ▾
Class mechanism. Coumarin-, salicylate- and coumestan-bearing botanicals add to vitamin-K-antagonist effect; several also compete for CYP2C9 and CYP3A4, raising S-warfarin exposure. Botanicals rich in vitamin K1 act in the opposite direction and blunt anticoagulation. Expected INR destabilisation in either direction; ecchymosis, epistaxis, gum bleeding, GI or intracranial haemorrhage. Management Do not start or stop the botanical without INR cover. Check INR at 3-5 days and again at 2 weeks. Document the product, batch and dose in the anticoagulation record. Onset rapid Evidence B - reviewed clinical column, source pending Matched on “anticoagulants” Find evidence for this pair Map this mechanism
Antidiabetic drugs (insulin, sulfonylureas, biguanides, GLP-1, SGLT2) Endocrine	3Major	PD-additive	curated B	Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events rep…	why ▾
Class mechanism. Hypoglycaemic botanicals act through insulin secretagogue, insulin-sensitising, alpha-glucosidase-inhibiting or glucose-transport routes. Added to a titrated pharmacological regimen the effects summate rather than plateau. Expected Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events reported with insulin and sulfonylureas. Management Increase self-monitoring frequency for 2 weeks after starting or stopping. Anticipate a downward dose adjustment of insulin or sulfonylurea. Onset rapid Evidence B - reviewed clinical column, source pending Matched on “hypoglycemic drugs” Find evidence for this pair Map this mechanism
Antiplatelet agents Haemostasis	3Major	PD-additive	curated B	Prolonged bleeding time, surgical and post-procedural bleeding, bruising,…	why ▾
Class mechanism. Organosulfur compounds, gingerols, salicylates, ginkgolides and eugenol inhibit thromboxane A2 synthesis, platelet aggregation and PAF-mediated activation, duplicating the pharmacology of aspirin and P2Y12 blockers. Expected Prolonged bleeding time, surgical and post-procedural bleeding, bruising, haematuria. Management Stop the botanical 7-14 days before elective surgery or neuraxial anaesthesia. Record it on the pre-operative medicines list. Onset rapid Evidence B - reviewed clinical column, source pending Matched on “antiplatelets” Find evidence for this pair Map this mechanism
NSAIDs Analgesia	3Major	PD-additive	curated B	Peptic ulceration, upper GI bleeding, acute kidney injury in volume-deple…	why ▾
Class mechanism. Salicylate-, coumarin- and eugenol-bearing botanicals add both antiplatelet activity and direct gastric mucosal irritation to cyclo-oxygenase inhibition; several also reduce renal prostaglandin-dependent perfusion. Expected Peptic ulceration, upper GI bleeding, acute kidney injury in volume-depleted patients. Management Avoid in ulcer history. Add gastroprotection where the combination is unavoidable, and monitor renal function in the elderly. Onset rapid Evidence B - reviewed clinical column, source pending Matched on “nsaids” Find evidence for this pair Map this mechanism
Antihypertensives Cardiovascular	2Moderate	PD-additive	curated B	Orthostatic hypotension, dizziness, syncope and falls; or loss of blood-p…	why ▾
Class mechanism. Vasodilator, diuretic, ACE-inhibitory and calcium-antagonist activity in botanical extracts adds to prescribed blood-pressure lowering. A minority (ephedrine-, glycyrrhizin- and caffeine-bearing) act in the opposite direction and antagonise control. Expected Orthostatic hypotension, dizziness, syncope and falls; or loss of blood-pressure control with pressor botanicals. Management Home BP log for 2 weeks after any change. Warn about postural symptoms; review in the elderly and in those on multiple agents. Onset rapid Evidence B - reviewed clinical column, source pending Matched on “antihypertensives” Find evidence for this pair Map this mechanism

Predicted from constituent chemistry

These edges are not clinical findings. Each one is a rule inference: a constituent class in this plant is known to act on a target that the drug class also acts on. They are shown because a blank cell reads as “safe”, and for a Tier 1 entry a blank cell only means “not yet looked at”. Treat them as a literature-search agenda, not as a warning.

Drug class	Severity	Mechanism type	Provenance	Expected effect
Cardiac glycosides (digoxin, digitoxin) Cardiovascular	4Contraindicated	PD-additive + PK-transporter + assay interference	predicted D	Nausea, xanthopsia, bradyarrhythmia, AV block, ventricular tachycardia an…	why ▾
Chemistry of this pair. Hydroxyanthracene derivatives are colonic prokinetics activated by gut flora; chronic use produces potassium loss through the colon. Class mechanism. Cardenolide- and bufadienolide-bearing plants are themselves Na+/K+-ATPase inhibitors, so co-administration is pharmacological overdose. Several also inhibit intestinal P-glycoprotein, raising digoxin exposure, and cross-react with digoxin immunoassays so that serum levels become uninterpretable. Expected Nausea, xanthopsia, bradyarrhythmia, AV block, ventricular tachycardia and death; falsely reassuring or falsely high assay results. Management Treat as an absolute contraindication. If exposure has occurred, manage on ECG and clinical grounds, not on assay values, and consult toxicology about digoxin-specific Fab. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Corticosteroids Endocrine	3Major	PD-additive + PK-CYP3A4	predicted D	Pseudohyperaldosteronism: hypertension, hypokalaemia, oedema, myopathy; C…	why ▾
Chemistry of this pair. Hydroxyanthracene derivatives are colonic prokinetics activated by gut flora; chronic use produces potassium loss through the colon. Class mechanism. Glycyrrhizin inhibits 11-beta-hydroxysteroid dehydrogenase type 2 and prolongs cortisol half-life, potentiating mineralocorticoid effect. Anthraquinone laxatives compound steroid-driven potassium loss, and CYP3A4 inhibition raises systemic corticosteroid exposure. Expected Pseudohyperaldosteronism: hypertension, hypokalaemia, oedema, myopathy; Cushingoid features at unchanged steroid dose. Management Restrict licorice-containing products. Check potassium and blood pressure. Reduce steroid dose if features of excess appear. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Diuretics Renal	3Major	PD-additive + electrolyte-mediated	predicted D	Hypokalaemia, hyponatraemia, dehydration, muscle weakness, cramps, arrhyt…	why ▾
Chemistry of this pair. Hydroxyanthracene derivatives are colonic prokinetics activated by gut flora; chronic use produces potassium loss through the colon. Class mechanism. Aquaretic and saluretic botanicals add to renal potassium and sodium loss. Anthraquinone laxatives compound this through colonic potassium loss, and glycyrrhizin causes mineralocorticoid-like retention of sodium with kaliuresis. Expected Hypokalaemia, hyponatraemia, dehydration, muscle weakness, cramps, arrhythmia; potentiation of digoxin toxicity through low potassium. Management Check potassium, sodium and creatinine 1-2 weeks after starting. Avoid the combination entirely in patients also on digoxin. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Laxatives and antidiarrhoeals Gastrointestinal	3Major	PD-additive	predicted D	Cramping, diarrhoea, electrolyte loss, melanosis coli with chronic anthra…	why ▾
Chemistry of this pair. Hydroxyanthracene derivatives are colonic prokinetics activated by gut flora; chronic use produces potassium loss through the colon. Class mechanism. Anthraquinone and mucilage botanicals add to stimulant and bulk laxative action; tannin-rich astringents oppose it. Expected Cramping, diarrhoea, electrolyte loss, melanosis coli with chronic anthraquinone use; or constipation and obstruction risk with astringents plus inadequate fluid. Management Limit stimulant laxative botanicals to under 2 weeks. Ensure adequate fluid intake with any bulk-forming product. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

05 Hazard register

The audit recorded no hazard beyond the interaction profile. The controlled-vocabulary field reads not assessed, which means the assessment has not been done rather than that it came back clear.

06 Confusable material

No same-genus or shared-common-name entry in the corpus.

07 Mechanism map

Chemistry sorts to the left, pharmacology to the right. Dashed edges are predicted. Drag nodes, scroll to zoom, export at 3× for a figure.

species

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marker compound

drug class

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hazard

08 Open literature

Abstract-scoped query built from this binomial, its common names and its marker compounds, run live against Europe PMC, PubMed and OpenAlex, then ranked locally against an evidence hierarchy.

Checking openFDA spontaneous reports…

09 Isomechanistic neighbours

Species whose interaction profile overlaps this one, ranked by shared severity weight rather than by count — a shared contraindication counts for more than a shared minor signal. Practical use: these are the plants you should not stack with this one, because the mechanisms summate.

Species	Family	Shared classes	Jaccard
Uncaria tomentosa Cat's Claw	Rubiaceae	7	0.44
Echinacea purpurea Echinacea	Asteraceae	6	0.35
Senna alexandrina Senna	Fabaceae	6	0.35
Aloe barbadensis Mill Aloe Vera	Asphodelaceae	6	0.43
Cyperus rotundus Nagarmotha	Cyperaceae	6	0.43
Garcinia indica Kokum	Clusiaceae	5	0.36

10 References and notes

No citation is on record for this entry. That is itself the finding: the audit flagged it, and it is why the entry does not carry an A evidence grade.

Curator notes

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